Burns & Trauma最新文献

{"title":"Masterful macrophages: understanding and targeting activation dysfunction in diabetic wounds","authors":"Linian Peng, Gaoxing Luo, Weifeng He, Guangping Liang","doi":"10.1093/burnst/tkaf003","DOIUrl":"https://doi.org/10.1093/burnst/tkaf003","url":null,"abstract":"Diabetes mellitus is a group of chronic metabolic diseases worldwide seriously threatens human health and increases social and economic burden; underlying drivers of impaired healing include uncontrolled inflammation, repeated ischemia–reperfusion injury, and neuropathy alongside infection risks. Macrophages orchestrate standard repair, exhibit sustained classical pro-inflammatory activation in diabetes, disrupting growth factor secretion, angiogenesis, and matrix regulation. Hyperglycemia- mediated advanced glycation end products and reactive oxygen species heighten pattern recognition receptor stimulation, causing reduced alternative macrophage differentiation. Promising immunomodulation approaches redirecting their phenotypes to resolve inflammation and stimulate regeneration provides optimism. We discuss macrophage origination, polarization dynamics, diabetic wound phenotypic imbalance, and critical microenvironmental disruptions perpetuating pathological function. Elucidating specific regulatory nodes upholding their activation states will inform intelligent targeting opportunities. Overall, infiltrating macrophages constitute indispensable yet amenable diabetic wound healing coordinators.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"11 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142992575","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A bioactive Hydrogel Patch Accelerates Revascularization in Ischemic Lesions for Tissue Repair","authors":"Zhuo Liu, Kang Wu, Hong Zeng, Wenxin Huang, Xuemeng Wang, Ying Qu, Chuntao Chen, Lei Zhang, Dongpin Sun, Sifeng Chen, Xiao Lin, Ning Sun, Lei Yang, Chen Xu","doi":"10.1093/burnst/tkaf005","DOIUrl":"https://doi.org/10.1093/burnst/tkaf005","url":null,"abstract":"Background Magnesium ions play crucial roles in maintaining cellular functions. Research has shown that Mg2+ can promote angiogenesis, indicating its potential for treating cardiovascular ischemic diseases. However, conventional intravenous or oral administration of Mg2+ presents several challenges, including the risk of systemic side effects, diminished bioavailability, and a lack of targeted delivery mechanisms. In this study, we designed a Mg2+-releasing adhesive tissue patch (MgAP) that enables the dural release of Mg2+ ions. Methods A novel Mg2+-releasing adhesive patch (MgAP) was developed on the basis of ionic crosslinking. Fourier transform infrared spectroscopy confirmed the chemical structure, whereas rheological analysis demonstrated stable mechanical properties and adaptability to dynamic loads. Sustained Mg2+ release was quantified over 7 days by inductively coupled plasma–mass spectrometry. In a rat acute myocardial infarction model, we performed echocardiography and strain analysis to assess cardiac function and histological staining to evaluate adverse remodeling. We also verified the proangiogenic effect through in vitro tube formation and in vivo immunofluorescence assays. Furthermore, transcriptomics and Western blotting were performed to explore the underlying mechanism. Additional assessments were also carried out in a rat model of lower limb ischemia. Results Compared with intravenous administration of magnesium chloride, MgAP application effectively improved cardiac function and reduced adverse remodeling in the myocardial infarction rat model. The left ventricular ejection fraction increased by 20.3 ± 6.6%, and the cardiac radial strain improved by 27.4 ± 4.1%. The cardiac fibrosis area and cell apoptosis rate decreased by 10.9 ± 1.2% and 32.1 ± 5.5%, respectively. RNA sequencing analysis also highlighted the upregulation of genes related to cardiac electrophysiological properties, structural and functional intercellular connections, and revascularization. The increased gap junction protein expression and restored local blood supply could contribute to the cardiac repair process posttreatment. The proangiogenic effect of MgAP was also observed in the rat limb ischemia model. Conclusions The above results revealed the convincing vascular regeneration effect of an ion therapy-based hydrogel, which enabled the local delivery of Mg2+ to the targeted ischemic tissue, aiding in cardiac and lower limb repair. This study presents a novel strategy and highlights its potential for use across various ischemic conditions.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"45 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142991903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Basic helix–loop–helix ARNT like 1 regulates the function of immune cells and participates in the development of immune-related diseases","authors":"Fanglin Shao, Zhipeng Wang, Luxia Ye, Ruicheng Wu, Jie Wang, Qing-Xin Yu, Dilinaer Wusiman, Zhouting Tuo, Koo Han Yoo, Ziyu Shu, Wuran Wei, Dengxiong Li, William C Cho, Zhihong Liu, Dechao Feng","doi":"10.1093/burnst/tkae075","DOIUrl":"https://doi.org/10.1093/burnst/tkae075","url":null,"abstract":"The circadian clock is an internal timekeeper system that regulates biological processes through a central circadian clock and peripheral clocks controlling various genes. Basic helix–loop–helix ARNT-like 1 (BMAL1), also known as aryl hydrocarbon receptor nuclear translocator-like protein 1 (ARNTL1), is a key component of the circadian clock. The deletion of BMAL1 alone can abolish the circadian rhythms of the human body. BMAL1 plays a critical role in immune cell function. Dysregulation of BMAL1 is linked to immune-related diseases such as autoimmune diseases, infectious diseases, and cancer, and vice versa. This review highlights the significant role of BMAL1 in governing immune cells, including their development, differentiation, migration, homing, metabolism, and effector functions. This study also explores how dysregulation of BMAL1 can have far-reaching implications and potentially contribute to the onset of immune-related diseases such as autoimmune diseases, infectious diseases, cancer, sepsis, and trauma. Furthermore, this review discusses treatments for immune-related diseases that target BMAL1 disorders. Understanding the impact of BMAL1 on immune function can provide insights into the pathogenesis of immune-related diseases and help in the development of more effective treatment strategies. Targeting BMAL1 has been demonstrated to achieve good efficacy in immune-related diseases, indicating its promising potential as a targetable therapeutic target in these diseases.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"49 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142988609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding the pathophysiology of Pseudomonas aeruginosa colonization as a guide for future treatment for chronic leg ulcers","authors":"Gabriela Gonzalez Matheus, Michelle N Chamoun, Kiarash Khosrotehrani, Yogeesan Sivakumaran, Timothy J Wells","doi":"10.1093/burnst/tkae083","DOIUrl":"https://doi.org/10.1093/burnst/tkae083","url":null,"abstract":"Chronic leg wounds represent a major burden of disease worldwide, costing health care systems billions of dollars each year. Aside from the financial implications, they also impose a significant physical and psychosocial burden on the patient, their relatives and/or carers, and the community. Whilst measures such as maintenance of wound hygiene, debridement, dressings and compression are the current standard of care, complete healing is not always achievable and ulcer recurrence is common. Thus, there is still a gap to breach in terms of understanding the intricate pathophysiology of chronic wounds and the role this plays on treatment and management. Pseudomonas aeruginosa has been linked to poor wound healing, with the pathogen being frequently isolated from chronic leg ulcers. Characterized by its multi-drug resistance, targeting P. aeruginosa requires the development of novel therapeutic options. Thus, the aim of this literature review is to describe the pathophysiology of P. aeruginosa in chronic leg ulcers and discuss novel treatment strategies. Here, we describe the key molecular mechanisms driving the observed clinical effect of P. aeruginosa on wounds and discuss novel strategies of molecular targeting of this common bacteria, establishing new approaches that could benefit patients with chronic hard to heal wounds.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"99 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142988610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Haemodynamic management of septic shock","authors":"Yuki Kotani, Nicholas Ryan, Andrew A Udy, Tomoko Fujii","doi":"10.1093/burnst/tkae081","DOIUrl":"https://doi.org/10.1093/burnst/tkae081","url":null,"abstract":"Septic shock is a significant challenge in the management of patients with burns and traumatic injuries when complicated by infection, necessitating prompt and effective haemodynamic support. This review provides a comprehensive overview of current strategies for vasopressor and fluid management in septic shock, with the aim to optimize patient outcomes. With regard to vasopressor management, we elaborate on the pharmacologic profiles and clinical applications of catecholamines, vasopressin derivatives, angiotensin II, and other vasoactive agents. Noradrenaline remains central to septic shock management. The addition of vasopressin, when sequentially added to noradrenaline, offers a non-catecholaminergic vasoactive effect with some clinical benefits and risks of adverse effects. Emerging agents such as angiotensin II and hydroxocobalamin are highlighted for their roles in catecholamine-resistant vasodilatory shock. Next, for fluid management, crystalloids are currently preferred for initial resuscitation, with balanced crystalloids showing benefits over saline. The application of albumin in septic shock warrants further research. High-quality evidence does not support large-volume fluid resuscitation, and an individualized strategy based on haemodynamic parameters, including lactate clearance and capillary refill time, is recommended. The existing knowledge suggests that early vasopressor initiation, particularly noradrenaline, may be critical in cases where fluid resuscitation takes inadequate effect. Management of refractory septic shock remains challenging, with novel agents like angiotensin II and methylene blue showing potential in recent studies. In conclusion, Further research is needed to optimize haemodynamic management of septic shock, particularly in developing novel vasopressor usage and fluid management approaches.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"75 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142986354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CYP24A1 is overexpressed in keloid keratinocytes and its inhibition alters profibrotic gene expression","authors":"Jennifer M Hahn, Kelly A Combs, Caitlin M Phillips, Petra M Warner, Uzair A Qazi, Heather M Powell, Dorothy M Supp","doi":"10.1093/burnst/tkae063","DOIUrl":"https://doi.org/10.1093/burnst/tkae063","url":null,"abstract":"Background Keloids are disfiguring, fibrotic scar-like lesions that are challenging to treat and commonly recur after therapy. A deeper understanding of the mechanisms driving keloid formation is necessary for the development of more effective therapies. Reduced vitamin D receptor (VDR) expression has been observed in keloids, implicating vitamin D signaling in keloid pathology. Vitamin D exhibits anti-proliferative and anti-inflammatory properties, suggesting it could have therapeutic utility in keloid disorder. The current study investigated vitamin D-regulated gene expression in keloid keratinocytes and the effects of inhibiting an enzyme involved in vitamin D metabolism on the phenotype of keloid-derived keratinocytes. Methods Normal and keloid-derived primary keratinocytes were isolated from normal skin and keloid lesions, respectively, and were cultured in the absence or presence of vitamin D. In some experiments, inhibitors of the vitamin D metabolizing enzyme CYP24A1, ketoconazole or VID400 were added in the absence or presence of vitamin D. Cellular proliferation, migration and gene expression were measured. Results We observed significant overexpression of CYP24A1 mRNA in keloid versus normal keratinocytes and increased CYP24A1 protein levels in keloids versus normal skin. CYP24A1 encodes 24 hydroxylase and is induced by vitamin D in a feedback loop that regulates vitamin D levels; thus, inhibition of CYP24A1 activity may locally increase active vitamin D levels. Ketoconazole, a non-specific cytochrome P-450 inhibitor, reduced proliferation of keloid and normal keratinocytes, but VID400, a specific CYP24A1 inhibitor, only significantly affected keloid keratinocyte proliferation. Neither inhibitor significantly reduced keratinocyte migration. The two inhibitors had different effects on vitamin D target gene expression in keratinocytes. Specifically, ketoconazole treatment reduced CYP24A1 expression in normal and keloid keratinocytes, whereas VID400 increased CYP24A1 expression. Both inhibitors decreased expression of profibrotic genes, including periostin and hyaluronan synthase 2, in keloid-derived cells. Combined treatment of keloid keratinocytes with vitamin D and ketoconazole or VID400 increased the effects of vitamin D treatment on target genes, although the effects were gene- and cell type-specific. Conclusions The data suggest that reduction of vitamin D inactivation with CYP24A1 inhibitors may reduce profibrotic gene expression in keloid-derived cells. Therefore, CYP24A1 inhibitors may serve as adjunctive therapies to suppress keloid-associated gene expression changes.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"29 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142987579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomarkers of sepsis in burn injury: an update","authors":"Tina L Palmieri, Jason Heard","doi":"10.1093/burnst/tkae080","DOIUrl":"https://doi.org/10.1093/burnst/tkae080","url":null,"abstract":"Sepsis, a dysregulated response to infection, is a leading cause of death after burn injury. Changes in the immune response as well as the loss of the skin, the primary barrier to infection, contribute to the increased risk for infection and sepsis in burn patients. This higher risk is further compounded by the development of the systemic inflammatory response and hypermetabolic state, which limit the utility of commonly used infection markers. As such, the development of sepsis biomarkers after burn injury is an imperative. A sepsis biomarker would facilitate earlier diagnosis and treatment of sepsis, thus decreasing length of stay, morbidity, and mortality after burn injury. Numerous different biomarkers, ranging from acute phase reactants, cytokines, and inflammatory markers to omics analyses and extracellular vesicles have been assessed as potential biomarkers in burn sepsis. To date no single biomarker has proven useful as the sole indicator for sepsis. The future of burn sepsis biomarkers will likely require a panel of biomarkers from all categories. The purpose of this review article is to list the various biomarkers that have been studied in burn sepsis and describe their clinical utility and future use in patients with burn injury.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"10 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142987584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The empowering influence of air-liquid interface culture on skin organoid hair follicle development","authors":"Jane Sun, Imaan Ahmed, Jason Brown, Kiarash Khosrotehrani, Abbas Shafiee","doi":"10.1093/burnst/tkae070","DOIUrl":"https://doi.org/10.1093/burnst/tkae070","url":null,"abstract":"Background Rodent models have been widely used to investigate skin development, but do not account for significant differences in composition compared to human skin. On the other hand, two-dimensional and three-dimensional engineered skin models still lack the complex features of human skin such as appendages and pigmentation. Recently, hair follicle containing skin organoids (SKOs) with a stratified epidermis, and dermis layer have been generated as floating spheres from human-induced pluripotent stem cells (hiPSCs). Methods The current study aims to investigate the generation of hiPSCs-derived SKOs using an air-liquid interface (ALI) model on transwell membranes (T-SKOs) and compares their development with conventional floating culture in low-attachment plates (F-SKOs). Results Mature SKOs containing an epidermis, dermis, and appendages are created in both T-SKO and F-SKO conditions. It was found that the hair follicles are smaller and shorter in the F-SKO compared with T-SKOs. Additionally, the ALI conditions contribute to enhanced hair follicle numbers than conventional floating culture. Conclusions Together, this study demonstrates the significant influence of transwell culture on the morphogenesis of hair follicles within SKOs and highlights the potential for refinement of skin model engineering for advancing dermatology and skin research.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"42 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142987583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipopolysaccharide-induced active telocyte exosomes alleviate lipopolysaccharide-induced vascular barrier disruption and acute lung injury via the activation of the miRNA-146a-5p/caspase-3 signaling pathway in endothelial cells","authors":"Xiaoqin Huang, Haoran Zhang, Yuhong Luo, Xin Yi, Zengding Zhou, Feng Guo, Lei Yi","doi":"10.1093/burnst/tkae074","DOIUrl":"https://doi.org/10.1093/burnst/tkae074","url":null,"abstract":"Background Lipopolysaccharide (LPS)-induced apoptosis of lung microvascular endothelial cells (ECs) is the main reason of lung edema and acute lung injury (ALI) in septic conditions. Telocytes (TCs) are a distinct type of interstitial cells found around the lung microvasculature, which may protect ECs through the release of shed vesicles. However, whether TCs protect against LPS-induced EC apoptosis and ALI has not been determined. Methods The protective effects of TCs on ECs were assessed in vitro using transwell assays and flow cytometry, and in vivo using an LPS-induced mouse ALI model. RNA sequencing was used to identify miRNA-146a-5p as a key component of TC-derived exosomes. The functions of miRNA-146a-5p were further evaluated by western blotting, flow cytometry, and transendothelial electrical resistance measurements. Results We demonstrated that LPS stimulation induced the secretion of active exosomes from TCs, which inhibited LPS-mediated apoptosis of ECs and reduced ALI in mice. Moreover, miRNA-146a-5p was identified as the main bioactive molecule in TC-derived exosomes, capable of inhibiting LPS-induced caspase-3 activation and apoptosis in ECs. Conclusions Our results indicate that TCs effectively prevent LPS-induced EC apoptosis and ALI through the release of exosomes, with subsequent activation of the miRNA-146a-5p/caspase-3 signaling pathway in ECs.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"42 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142981461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The pathogenesis and management of heatstroke and heatstroke-induced lung injury","authors":"Jian Liu, Qin Li, Zhimin Zou, Li Li, Zhengtao Gu","doi":"10.1093/burnst/tkae048","DOIUrl":"https://doi.org/10.1093/burnst/tkae048","url":null,"abstract":"In the past two decades, record-breaking heat waves have caused an increasing number of heat-related deaths, including heatstroke, globally. Heatstroke is a life-threatening systemic condition characterized by a core body temperature >40°C and the subsequent development of multiple organ dysfunction syndrome. Lung injury is a well-documented complication of heatstroke and is usually the secondary cause of patient death. In recent years, extensive research has been conducted to investigate the underlying causes of heatstroke and heatstroke-induced lung injury. This review aims to consolidate and present the current understanding of the key pathogenic mechanisms involved in heatstroke and heatstroke-induced lung injury. In addition, systemic factors such as heat cytotoxicity, systemic inflammation, oxidative stress, endothelial cell dysfunction, and other factors are involved in the pathogenesis of lung injury in heatstroke. Furthermore, we also established current management strategies for heatstroke and heatstroke-induced lung injury. However, further investigation is required to fully understand the detailed pathogenesis of heatstroke so that potentially effective means of treating and preventing heatstroke and heatstroke-induced lung injury can be developed and studied.","PeriodicalId":9553,"journal":{"name":"Burns & Trauma","volume":"1 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142981463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}